DESCRIPTION: This proposal focuses on the mechanism of regulation and execution of a pathogen-triggered cell death program called the hypersensitive response (HR) in plants. The HR is part of a rapidly deployed defense response which functions to limit the spread of a pathogenic infection. Previously, a strategy was developed to study mechanism of HR control. The investigator isolated Arabidopsis plants which, due to single gene mutations, are able to bypass pathogen exposure to activate the HR and additional defenses. Plants harboring these mutations (called acd2 for accelerated cell death) show the HR, but harbor no infections agents. Since the acd2 mutations are recessive, the investigator's model is that ACD2 negatively regulates the HR and multiple defense functions. To understand the regulation and execution of the HR, the specific goals of this project are: to clone and characterize the ACD2 gene and its product, to identify the likely cell death inducing and regulatory genes under ACD2 control, and to identify additional genes that interact with ACD2 in the cell death regulatory pathway. Recent studies in the field of pathogenesis suggest that certain plant and animal pathogens have common pathogenicity genes. On the host side, both plant and animal cells can undergo programmed cell death during pathogen attack. The possibility exists that similar mechanisms of regulation and execution of cell death are used by both plants and animals. The ability to do genetics, molecular biology and biochemistry with both the pathogen and the host makes the study of host- pathogen interactions using the model system of Arabidopsis and Pseudomonas attractive for elucidating the mechanism and role of pathogen-induced cell death. In addition to activating the HR, the acd2 mutants activate at least two other defense pathways that are usually triggered only after certain pathogens infect wild-type plants. These pathways require two signals: the known signal molecule salicylic acid and an as yet uncharacterized signal. The long term goals of this work are to understand how these pathways are coordinately regulated by the ACD2-controlled signal(s), how the cell death program is activated and how the components of the signal transduction pathway(s) activate ACD2-controlled defenses.